The basis for the exaggerated release of substrates for gluconeogenesis and other caloric fuels in Reye's syndrome, a pediatric disorder characterized by encephalopathy and fatty visceral changes, will continue to be explored using the fat cell as a model system since excessive lipolysis is a prominent feature of this disorder. The process of lipolysis is being studied in biopsied tissues and the sequential steps involved in the transmission of a lipolytic stimulus are being examined and compared in control and Reye's samples. The molecular forms of the liver phosphodiesterases are being isolated, characterized and compared between affected and age-matched controls. Pancreatic endocrine responses to various modulators in survivors and their families are under investigation to determine the basis for the altered responsiveness to metabolic stress observed in survivors and some members of their families.